Gestational diabetes mellitus (GDM) and pre-gestational diabetes are known to pose risks to the mother and developing fetus, often related to abnormal fetal growth. One potential mediator of maternal effects on fetal growth is Placental Growth Hormone (PGH). PGH is produced by the syncytiotrophoblast and found predominantly in the maternal circulation. It progressively replaces pituitary growth hormone (hGH) in the human maternal circulation from midgestation onwards, peaking towards term. PGH appears to be an important potential regulator of maternal insulin resistance in human pregnancy and may influence fetal growth both by modifying substrate availability and through paracrine actions in the placental bed. The details of PGH regulation remain relatively poorly understood, but current evidence does suggest a central role in growth restricted pregnancies. There is currently less evidence of a pathophysiologic role in production of the macrosomic fetal phenotype commonly seen in response to hyperglycaemia, although our recent in vitro studies do raise the possibility of feto-placental feedback as a mechanism of growth modulation.